Neuroendocrine tumors (NETs) harbor somatostatin receptors and there is a strong rationale for using somatostatin analogs (SSAs) for treatment of NETs. Areas covered: This article discusses i) pharmacology of somatostatin and its analogs; ii) antisecretory and anti-proliferative effects of SSAs in NETs; iii) efficacy and safety of emerging therapeutic regimens with first generation SSAs administered at either high doses or in combination with antineoplastic drugs; iv) efficacy and safety of pasireotide and chimeric molecules; v) efficacy of radionuclide therapy of NETs using SSAs. Expert opinion: SSAs are the first-line medical therapy for functioning and non-functioning well-differentiated NETs. In patients not responder to first generation SSAs, the increase of drug dose over the conventional regimens, the combination of SSAs with other biotherapies or molecular targeted therapies, the switch to pasireotide or the use of SSAs in radionuclide therapy may improve the therapeutic success.

Multiple endocrine neoplasia type 1 (MEN1) is a hereditary syndrome associated with the development of many endocrine tumors, involving mainly pituitary, parathyroids, pancreas, although a proliferative state interests all neuroendocrine system. MEN1 pancreatic neuroendocrine tumors (pNETs) are multiples and can secrete different hormones. The therapeutic approach is based on surgery which usually is followed by tumor relapse or persistence unless to be highly aggressive. Biotherapy with somatostatin analogs and dopamine agonists could be of great benefit to manage these patients without altering their life quality. We report a case of a 36-year-old MEN1 man affected with multicentric pNETs associated with insulinoma syndrome. Therapy with symptomatic agents (diazoxide), as well as biotherapy (lanreotide, cabergoline) was started. At 6-month follow-up, symptomatic agents were stopped and disease control was only based on lanreotide plus cabergoline. This combined biotherapy was able to control endocrine syndromes and tumor growth. Subsequently, a safer and selective surgical intervention on pNETs was performed. An excellent response to therapy with lanreotide autogel and cabergoline has been observed in a MEN1 patient with pNETs associated with insulinoma syndrome. The potential synergistic effects of lanreotide autogel and cabergoline on insulin-secreting neuroendocrine tumors are discussed.

Severe or morbid obesity, with body mass indexes exceeding 35 to 40, are often refractory to all therapies other than surgery. The increasing number of patients undergoing bariatric surgery will result in increasing numbers of patients with gastrointestinal complications. The types of complications vary with type of surgery, whether restrictive, malabsorptive, or both, depending on what anatomical and physiologic changes occur postoperatively. One complication of bariatric surgery (gallstones) is due to weight loss after surgery, not the surgery itself. Based on previous meta-analyses, most of the top 10 complications from bariatric surgery are gastrointestinal: dumping, vitamin/mineral deficiencies, vomiting (and nausea), staple line failure, infection, stenosis (and bowel obstruction), ulceration, bleeding, splenic injury, and perioperative death. Two other gastrointestinal complications of bariatric surgery are indirect consequences of the surgery: bacterial overgrowth and diarrhea. Awareness of the types and frequency of gastrointestinal complications of bariatric surgery allows for timely diagnosis and appropriate therapy. As new surgical, and even endoscopic, procedures to treat obesity are developed, new gastrointestinal complications will need to be recognized.

Unfortunately normal gastrointestinal function after an esophagectomy is rare. Most patients will never eat the way they did before their illness. Most patients require smaller more frequent meals. It is common for patients to loose up to 15% of their body weight from the time of diagnosis through the first 6 months postoperatively, but fortunately this trend levels off after 6 months. Dumping syndrome, delayed gastric emptying, reflux, and dysphagia can all contribute to nutritional deficiency and poor quality of life. There is no one surgical modification to eliminate any one of these complications, but several guidelines can help reduce conduit dysfunction. Most patients seem to benefit from a 5-cm-wide greater-curvature gastric tube brought up through the posterior mediastinum. The gastric-esophageal anastomosis should be placed higher than the level of the azygous vein. Drainage procedures seem to be helpful, especially when using the whole stomach as a conduit. Early erythromycin therapy significantly aids in the function of the gastric conduit. Proton-pump inhibitors are important for improvement of postoperative reflux symptoms and to help prevent Barrett's metaplasia in the esophageal remnant. Single-layer hand-sewn or semi-mechanical anastomoses provide greater cross-sectional area and fewer problems with stricture. When benign strictures occur, early endoscopy and dilation with proton-pump inhibition greatly reduces the morbidity. Patients should be instructed to eat six small meals a day and to remain upright for as long as possible after eating. Simple sugars and fluid at mealtime should be avoided until the function of the conduit is established.

Anatomic and physiologic changes introduced by gastric surgery result in clinically significant dumping syndrome in approximately 10% of patients. Dumping is the effect of alteration in the motor functions of the stomach, including disturbances in the gastric reservoir and transporting function. Gastrointestinal hormones play an important role in dumping by mediating responses to surgical resection. Treatment options of dumping syndrome include diet, medications, and surgical revision. Poor nutrition status can be anticipated in patients who fail conservative therapy. Management of refractory dumping syndrome can be a challenge. This review highlights current knowledge about the mechanisms of dumping syndrome and available therapy.

Somatostatin is produced in enteroendocrine D cells and intrinsic neurons of the stomach, intestines and pancreas. Its physiologic actions are mediated primarily by somatostatin receptors type 2 and 5, and include the inhibition of secretion of most endocrine and exocrine factors. Diseases directly attributable to somatostatin excess or deficiency are rare, although there is a complex pathogenic relationship between persistent Helicobacter pylori infection and reduced somatostatin in chronic gastritis. Abundant somatostatin receptors on many neoplastic and inflammatory cells are the basis for sensitive in vivo imaging with radiolabeled somatostatin analogs and provide a therapeutic target. Current indications for somatostatin therapy include hormone-expressing neuroendocrine tumors, intractable diarrhea and variceal bleeding secondary to portal hypertension. Exciting advances are being made in the development of high-affinity nonpeptide analogs with receptor-subtype selectivity and increased bioavailability. Somatostatin analogs coupled to high-energy radionuclides show promise as novel cytotoxic agents for certain metastatic tumors.

The purpose of this study was to determine the significance and frequency of rapid gastric emptying (RGE) in clinical practice and to examine its relationship to age, gender, and presenting symptoms.

The review included 750 patients who underwent scintigraphic gastric emptying studies (GES) within the past 11 years. In 80 patients with RGE, the mean gastric emptying time (GET) in female and male patients was compared with study gender differences. Similarly, the mean GET in young and old patients was compared with study age differences. The presenting symptoms and conditions indicating GES were noted.

RGE was found in 80 of 750 study patients (10.7%). RGE was equally common in both sexes. Younger patients (mean age, 34.3 +/- 9.5 years) and older patients (mean age, 67.3 +/- 11.6 years) had similar mean GETs. Most patients with RGE presented with symptoms that mimicked gastroparesis.

RGE has no relationship to age or gender. RGE may be representative of early dumping syndrome in most patients. GES help make a clear distinction between early dumping syndrome and gastroparesis, which can present with similar symptoms.

The inhibitory peptide hormone somatostatin and its receptors (sst1-sst5) regulate many physiological functions in the gastrointestinal tract. In an attempt to correlate the various effects of somatostatin in gastrointestinal physiology to individual sst subtypes sst1-sst5, mRNAs have been localized by semiquantitative reverse transcription polymerase chain reaction amplification and in situ hybridization of sst1 and sst3 in the rat alimentary tract. sst1-sst4 mRNAs were found throughout the gastrointestinal tract, sst1 mRNA being more abundant than sst2 and much more abundant than sst3 and sst4 mRNAs. sst5 transcripts were at the detection threshold. sst1 and sst3 mRNAs are present in enterocytes and enteric neurons suggesting a role of these subtypes in the somatostatin-mediated inhibition of acetylcholine release from myenteric neurons and of secretomotor neuron activity in the submucous plexus. The presence of sst3 mRNA in smooth muscle cells points to an additional role of this receptor in regulating gut motility.